The proinflammatory cytokine Interleukin-1β (IL-1β), which increased in the heart post myocardial infarction (MI), has been shown to cause a loss of Connexin43 (Cx43)-mediated gap junctional coupling, an event known to underlie formation of the arrhythmogenic substrate.Omega 3 Fatty acids exhibit antiarrhythmic properties and impact on IL1β signaling.We now show that Omega-3 fatty acids prevent arrhythmias in part by inhibiting IL-1β signaling thus maintaining functional gap junction channels.Omega 3 Fatty acid treatment inhibited IL-1 β-stimulated loss of Cx43 by alters the transcription factors involved in the IL-lb pathway.These data suggest that the cardio-protective mechanisms by which Omega 3 Fatty acids work include prevention of the proarrhythmic loss of Cx43 by dampening the inflammatory response to an MI.